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Ascending Aortic Pseudoaneurysm
Ascending Aortic Pseudoaneurysm Michael Ingoglia, MD, Saroj Pani, MD, Lewis Britton, MD, Marcela Hanakova, MD, Asim Raja, MD, Kody El-Mohtar, MD, and Farhan Sheikh, MD, FASE
A
SCENDING AORTIC pseudoaneurysms are rare entities that can occur secondary to trauma, infection, connective tissue disorders, vasculitis, or as a complication of cardiac surgery. The most common predisposing cause is aortic root surgery followed by coronary artery bypass graft surgery; they are well-known complications after any cardiac surgery although ascending aortic pseudoaneurysms occur in less than 0.5% of all cardiac surgical cases.1 This complication carries a significant early morbidity and mortality rate near 20% and a yearly mortality rate as high as 40% and usually requires immediate surgical intervention as ascending aortic pseudoaneurysms are prone to rupture.2,3 They may be seen as early or late complications of cardiac surgery and may be seen as late as 20 years or more after the original surgery. The most frequent site of pseudoaneurysm formation is in areas of aortic wall disruption, most commonly seen at the aortic cannulation site, but also may occur at the saphenous vein graft site, aortotomy site, or the aortic vent site.4,5 Few studies have addressed this rare complication aside from a handful of case studies and a few small retrospective studies. A pseudoaneurysm, or false aneurysm, is essentially a contained rupture. It is caused by a defect in the vessels’ inner layers, the tunica intima and the tunica media, with an intact tunica adventitia, or it can involve all 3 layers in which the blood flow is contained by surrounding structures although in true aneurysms all 3 layers remain intact. Of the infectious causes of aortic pseudoaneurysms, Staphylococcus aureus is the most common. Other infectious causes of aortic pseudoaneurysms include Staphylococcus epidermidis, Proprionibacterium acnes, Pseudomonas aeruginosa, Enterobacter, Serratia, Streptococcus pyogenes, tuberculosis, and Candida species causing mycotic pseudoaneurysms, which usually are seen in the immunosuppressed after heart or heart-lung transplant. Infection also has been found to play a significant role in the development of ascending aortic pseudoaneurysms after cardiac surgery. CASE REPORT A 57-year-old man presented to the emergency department with nonradiating substernal chest pain that woke him in the middle of the night. The chest pain was notably worse when lying down and relieved to a small degree by sitting forward. He also complained of chills and low-grade fevers and stated that this chest pain has been intermittent but persistent over the past 3 days and had been getting progressively worse. His medical history was significant for hypertension, hypercho-
From the Department of Anesthesiology, Albany Medical Center, Albany, NY. Address reprint requests to Michael Ingoglia, MD, Albany Medical Center Department of Anesthesiology, 43 New Scotland Avenue, Mail Code 131, Albany, NY 12208. E-mail: [email protected] © 2011 Elsevier Inc. All rights reserved. 1053-0770/2506-0033$36.00/0 doi:10.1053/j.jvca.2010.09.003 Key words: aortic pseudoaneurysm, pericarditis, methicillin-sensitive staphylococcus aureus 1098
lesterolemia, chronic renal insufficiency, chronic obstructive pulmonary disease, and a continued 40-pack-year smoking history. Approximately 4 months earlier, he had presented to another facility with similar substernal chest pain worsened on exertion. A cardiac workup including cardiac enzymes and troponin ruled out myocardial infarction. A presumptive diagnosis of pericarditis was made based on electrocardiograms that showed diffuse ST elevations. The chest x-ray showed calcifications of the thoracic aorta. A transthoracic echocardiogram (TTE) did not show pericardial effusion. He ultimately was discharged and treated with a nonsteroidal anti-inflammatory and colchicine. He returned approximately 3 weeks later to the authors’ facility with similar symptoms despite nonsteroidal anti-inflammatory drug and colchicine use. He underwent a diagnostic and interventional left-heart catheterization that showed a 90% lesion in the mid–left anterior descending coronary artery for which a drug-eluting stent was placed in the left anterior descending artery. There was heavy calcification of the ascending aorta. No aortogram was performed at this time. The procedure was uneventful. There was no injury to the aortic wall at that time. He was discharged and given a follow-up appointment. He returned to the hospital several more times over the next month with similar chest pain episodes. Despite continued treatment with oxacillin and steroid regimens, the patient progressed to develop significant pericardial effusions visualized by a TTE, requiring pericardial windows for drainage on 2 separate occasions; the first performed via a subxiphoid approach and the second by a left minithoracotomy 2 weeks later. Cloudy fluid was drained at the first operation. Pericardial fluid cultures grew methicillin-sensitive S aureus. The second pericardial window was performed through a left thoracotomy approach because the pericardial fluid was believed to be loculated and showed old clotted blood. Because of persisting chest pain and after ruling out coronary insufficiency, a CT chest scan was performed without contrast because of his chronic renal insufficiency. This study showed an ill-defined density behind the ascending aorta. The differential diagnosis at this time was either a loculated pleural effusion and/or an aortic pseudoaneurysm. For better visualization of the affected area, a transesophageal echocardiogram (TEE) was performed that showed minimal pericardial fluid and a large pseudoaneurysm of the ascending aorta. It showed a communication between the pseudoaneurysm and the ascending aorta. To get a clearer image of the site, a CT angiogram of the chest was performed. This revealed a pseudoaneurysm arising from the right posterolateral aspect of the proximal aorta at the level of the coronary sinus, measuring 8.8 cm ⫻ 4.7 cm, compressing the posterolateral wall of the ascending aorta, right pulmonary artery, and the inferior vena cava (Fig 1). There was also a loculated pericardial effusion measuring approximately 3.3 cm anteriorly ⫻ 2.2 cm posteriorly. The patient had renal insufficiency worsened by the contrast load. The authors allowed a period of time for renal function to stabilize before taking him to the operating room and placing him under general anesthesia. A TEE was performed intraoperatively that clearly visualized the pseudoaneurysm (Fig 2 and Videos 1 and 2 [supplementary videos are available online]). In addition to the fistula between the aorta and the pseudoaneurysm, a TEE also showed a communicating fistula between the pseudoaneurysm and the superior vena cava (SVC) (Fig 3). Surgery confirmed the fact that the patient had a controlled ascending aortic rupture, with erosion into the SVC. A diagnosis of endocarditis was established; therefore, all obvious infected material was to be excised. There was no indication for root replacement because the aortic valve was not involved and functionally normal. Current data do not support any advantage of homograft over other prosthetic material if adequate debridement and antibiotic prophylaxis are performed. The
Journal of Cardiothoracic and Vascular Anesthesia, Vol 25, No 6 (December), 2011: pp 1098-1100
ASCENDING AORTIC PSEUDOANEURYSM
1099
Fig 3. The TEE of the communicating fistula to the SVC with color Doppler. LA, left atrium; RA, right atrium; RV, right ventricle.
Fig 1. The CT chest scan with intravenous contrast. P, pseudoaneurysm; Ao, aorta.
patient underwent resection of the ascending aorta with cardiopulmonary bypass and deep hypothermic circulatory arrest and replacement of the ascending aorta with a 26-mm Hemashield tube graft and patch closure of the SVC fistula with a bovine pericardial patch. He was transferred to the cardiopulmonary surgical intensive care unit after a relatively uneventful surgical course and was discharged 9 days after surgery. DISCUSSION
Ascending aortic pseudoaneurysm is a rare but potentially fatal entity that occurs most commonly after cardiac surgery. Other causes include trauma, infection, connective tissue disorders, and vasculitis. Clinical presentation can vary significantly and range from the asymptomatic to fulminant sepsis. Other signs and symptoms include chest pain related to myo-
Fig 2. The TEE of the ascending aortic pseudoaneurysm. P, pseudoaneurysm; Ao, aorta; LV, left ventricle; LA, left atrium.
cardial ischemia, heart failure secondary to valvular regurgitation or cardiac compression, dysphagia, stridor, hoarseness caused by recurrent laryngeal nerve damage or compression, hemoptysis because of aortobronchial fistula, and embolic events associated with endocarditis.4 The most common predisposing factor for the development of an ascending aortic pseudoaneurysm is previous cardiac surgery; however, there have been sporadic cases of pseudoaneurysm formation without a history of cardiac surgery or a history of blunt chest trauma. These cases of pseudoaneurysm formation invariably have an infectious component involved, whether it is endocarditis, aortitis, or pericarditis.1 In a small retrospective study by Atik et al6 in 2006, they found that up to one third of all patients who developed a pseudoaneurysm of the thoracic aorta had endocarditis. In a study by Sullivan et al,4 they found that 18 of 31 cases of ascending aortic pseudoaneurysms in their review had a suspected or documented infection, suggesting that infection plays a significant role in pseudoaneurysm formation whether it follows cardiac surgery or infection is the primary cause. In a case study by Aranda et al2 in 1998, they showed an ascending thoracic pseudoaneurysm in a patient who presented with purulent pericarditis, which is similar to the present case report. There also have been documented cases of staphylococcus aortitis leading to pseudoaneurysm formation. This patient likely developed a pseudoaneurysm secondary to his recurrent methicillin-sensitive S aureus pericarditis and/or repeated pericardial surgeries. With the patient having significant symptoms over an extended time period with unresolving pericarditis despite appropriate treatment and recurring pericardial effusions, it is most likely that the infectious pericarditis was the precipitating event or an atheromatous ulcer became infected causing the pseudoaneurysm. A chest CT scan, magnetic resonance imaging, aortography, and transesophageal echocardiography are very reliable in detecting aortic pseudoaneurysms, and TEE has been shown to be highly sensitive and specific for diagnosing pseudoaneurysm formation. Transthoracic echocardiography is a less reliable method for diagnosing thoracic pseudoaneurysm because there
1100
INGOGLIA ET AL
frequently can be interference from the lung, ribs, and subcutaneous tissues depending on the patient’s body habitus. The TEE affords much better resolution because transduction is not obscured by dense surrounding tissues and its relative proximity to the ascending aorta.7 In a patient who has had cardiac surgery, regardless of how remote, who presents with chest pain and other related symptoms that cannot be explained by electrocardiogram and laboratory findings should be further investigated, especially if any
of the afore mentioned symptoms are present. Nonresolving pericarditis after an extended treatment course may warrant imaging studies other than a TTE to gain clear visualization of the heart and surrounding structures that a TTE can miss. Although the incidence of thoracic pseudoaneurysm formation in patients without prior cardiac surgery is very low, pseudoaneurysm should be a consideration after other more common diagnoses are excluded.
REFERENCES 1. Dumont E, Carrier M, Cartier R, et al: Repair of aortic false aneurysm using deep hypothermic and circulatory arrest. Ann Thorac Surg 78:117-120, 2004 2. Aranda J, Tauth J, Henning RJ, et al: Pseudoaneurysm of the thoracic aorta presenting as purulent pericarditis and pericardial effusion. Cathet Cardiovasc Diagn 43:63-67, 1998 3. Sequeira de Almeida RM, Limas JD, Kahrbek T, et al: Surgical repair of a pseudoaneurysm of the ascending aorta after aortic valve replacement. Arq Bras Cardiol 76:326-328, 2001
4. Sullivan KL, Steiner RM, Smullens SL, et al: Pseudoaneurysm of the ascending aorta following cardiac surgery. Chest 93:138-143, 1988 5. Konia M, Uppington J, Moore P, et al: Ascending aortic pseudoaneurysm: A late complication of coronary artery bypass. Anesth Analg 106:767-768, 2008 6. Atik FA, Navia JL, Svensson LG, et al: Surgical treatment of pseudoaneurysm of the thoracic aorta. J Thorac Cardiovasc Surg 132:379385, 2006 7. Lobato EB, McKenzie ED, Beaver TM: Intraoperative diagnosis of aortic pseudoaneurysm with transesophageal echocardiography. J Clinical Monit Comput 15:53-55, 1999
A
SCENDING AORTIC pseudoaneurysms are rare entities that can occur secondary to trauma, infection, connective tissue disorders, vasculitis, or as a complication of cardiac surgery. The most common predisposing cause is aortic root surgery followed by coronary artery bypass graft surgery; they are well-known complications after any cardiac surgery although ascending aortic pseudoaneurysms occur in less than 0.5% of all cardiac surgical cases.1 This complication carries a significant early morbidity and mortality rate near 20% and a yearly mortality rate as high as 40% and usually requires immediate surgical intervention as ascending aortic pseudoaneurysms are prone to rupture.2,3 They may be seen as early or late complications of cardiac surgery and may be seen as late as 20 years or more after the original surgery. The most frequent site of pseudoaneurysm formation is in areas of aortic wall disruption, most commonly seen at the aortic cannulation site, but also may occur at the saphenous vein graft site, aortotomy site, or the aortic vent site.4,5 Few studies have addressed this rare complication aside from a handful of case studies and a few small retrospective studies. A pseudoaneurysm, or false aneurysm, is essentially a contained rupture. It is caused by a defect in the vessels’ inner layers, the tunica intima and the tunica media, with an intact tunica adventitia, or it can involve all 3 layers in which the blood flow is contained by surrounding structures although in true aneurysms all 3 layers remain intact. Of the infectious causes of aortic pseudoaneurysms, Staphylococcus aureus is the most common. Other infectious causes of aortic pseudoaneurysms include Staphylococcus epidermidis, Proprionibacterium acnes, Pseudomonas aeruginosa, Enterobacter, Serratia, Streptococcus pyogenes, tuberculosis, and Candida species causing mycotic pseudoaneurysms, which usually are seen in the immunosuppressed after heart or heart-lung transplant. Infection also has been found to play a significant role in the development of ascending aortic pseudoaneurysms after cardiac surgery. CASE REPORT A 57-year-old man presented to the emergency department with nonradiating substernal chest pain that woke him in the middle of the night. The chest pain was notably worse when lying down and relieved to a small degree by sitting forward. He also complained of chills and low-grade fevers and stated that this chest pain has been intermittent but persistent over the past 3 days and had been getting progressively worse. His medical history was significant for hypertension, hypercho-
From the Department of Anesthesiology, Albany Medical Center, Albany, NY. Address reprint requests to Michael Ingoglia, MD, Albany Medical Center Department of Anesthesiology, 43 New Scotland Avenue, Mail Code 131, Albany, NY 12208. E-mail: [email protected] © 2011 Elsevier Inc. All rights reserved. 1053-0770/2506-0033$36.00/0 doi:10.1053/j.jvca.2010.09.003 Key words: aortic pseudoaneurysm, pericarditis, methicillin-sensitive staphylococcus aureus 1098
lesterolemia, chronic renal insufficiency, chronic obstructive pulmonary disease, and a continued 40-pack-year smoking history. Approximately 4 months earlier, he had presented to another facility with similar substernal chest pain worsened on exertion. A cardiac workup including cardiac enzymes and troponin ruled out myocardial infarction. A presumptive diagnosis of pericarditis was made based on electrocardiograms that showed diffuse ST elevations. The chest x-ray showed calcifications of the thoracic aorta. A transthoracic echocardiogram (TTE) did not show pericardial effusion. He ultimately was discharged and treated with a nonsteroidal anti-inflammatory and colchicine. He returned approximately 3 weeks later to the authors’ facility with similar symptoms despite nonsteroidal anti-inflammatory drug and colchicine use. He underwent a diagnostic and interventional left-heart catheterization that showed a 90% lesion in the mid–left anterior descending coronary artery for which a drug-eluting stent was placed in the left anterior descending artery. There was heavy calcification of the ascending aorta. No aortogram was performed at this time. The procedure was uneventful. There was no injury to the aortic wall at that time. He was discharged and given a follow-up appointment. He returned to the hospital several more times over the next month with similar chest pain episodes. Despite continued treatment with oxacillin and steroid regimens, the patient progressed to develop significant pericardial effusions visualized by a TTE, requiring pericardial windows for drainage on 2 separate occasions; the first performed via a subxiphoid approach and the second by a left minithoracotomy 2 weeks later. Cloudy fluid was drained at the first operation. Pericardial fluid cultures grew methicillin-sensitive S aureus. The second pericardial window was performed through a left thoracotomy approach because the pericardial fluid was believed to be loculated and showed old clotted blood. Because of persisting chest pain and after ruling out coronary insufficiency, a CT chest scan was performed without contrast because of his chronic renal insufficiency. This study showed an ill-defined density behind the ascending aorta. The differential diagnosis at this time was either a loculated pleural effusion and/or an aortic pseudoaneurysm. For better visualization of the affected area, a transesophageal echocardiogram (TEE) was performed that showed minimal pericardial fluid and a large pseudoaneurysm of the ascending aorta. It showed a communication between the pseudoaneurysm and the ascending aorta. To get a clearer image of the site, a CT angiogram of the chest was performed. This revealed a pseudoaneurysm arising from the right posterolateral aspect of the proximal aorta at the level of the coronary sinus, measuring 8.8 cm ⫻ 4.7 cm, compressing the posterolateral wall of the ascending aorta, right pulmonary artery, and the inferior vena cava (Fig 1). There was also a loculated pericardial effusion measuring approximately 3.3 cm anteriorly ⫻ 2.2 cm posteriorly. The patient had renal insufficiency worsened by the contrast load. The authors allowed a period of time for renal function to stabilize before taking him to the operating room and placing him under general anesthesia. A TEE was performed intraoperatively that clearly visualized the pseudoaneurysm (Fig 2 and Videos 1 and 2 [supplementary videos are available online]). In addition to the fistula between the aorta and the pseudoaneurysm, a TEE also showed a communicating fistula between the pseudoaneurysm and the superior vena cava (SVC) (Fig 3). Surgery confirmed the fact that the patient had a controlled ascending aortic rupture, with erosion into the SVC. A diagnosis of endocarditis was established; therefore, all obvious infected material was to be excised. There was no indication for root replacement because the aortic valve was not involved and functionally normal. Current data do not support any advantage of homograft over other prosthetic material if adequate debridement and antibiotic prophylaxis are performed. The
Journal of Cardiothoracic and Vascular Anesthesia, Vol 25, No 6 (December), 2011: pp 1098-1100
ASCENDING AORTIC PSEUDOANEURYSM
1099
Fig 3. The TEE of the communicating fistula to the SVC with color Doppler. LA, left atrium; RA, right atrium; RV, right ventricle.
Fig 1. The CT chest scan with intravenous contrast. P, pseudoaneurysm; Ao, aorta.
patient underwent resection of the ascending aorta with cardiopulmonary bypass and deep hypothermic circulatory arrest and replacement of the ascending aorta with a 26-mm Hemashield tube graft and patch closure of the SVC fistula with a bovine pericardial patch. He was transferred to the cardiopulmonary surgical intensive care unit after a relatively uneventful surgical course and was discharged 9 days after surgery. DISCUSSION
Ascending aortic pseudoaneurysm is a rare but potentially fatal entity that occurs most commonly after cardiac surgery. Other causes include trauma, infection, connective tissue disorders, and vasculitis. Clinical presentation can vary significantly and range from the asymptomatic to fulminant sepsis. Other signs and symptoms include chest pain related to myo-
Fig 2. The TEE of the ascending aortic pseudoaneurysm. P, pseudoaneurysm; Ao, aorta; LV, left ventricle; LA, left atrium.
cardial ischemia, heart failure secondary to valvular regurgitation or cardiac compression, dysphagia, stridor, hoarseness caused by recurrent laryngeal nerve damage or compression, hemoptysis because of aortobronchial fistula, and embolic events associated with endocarditis.4 The most common predisposing factor for the development of an ascending aortic pseudoaneurysm is previous cardiac surgery; however, there have been sporadic cases of pseudoaneurysm formation without a history of cardiac surgery or a history of blunt chest trauma. These cases of pseudoaneurysm formation invariably have an infectious component involved, whether it is endocarditis, aortitis, or pericarditis.1 In a small retrospective study by Atik et al6 in 2006, they found that up to one third of all patients who developed a pseudoaneurysm of the thoracic aorta had endocarditis. In a study by Sullivan et al,4 they found that 18 of 31 cases of ascending aortic pseudoaneurysms in their review had a suspected or documented infection, suggesting that infection plays a significant role in pseudoaneurysm formation whether it follows cardiac surgery or infection is the primary cause. In a case study by Aranda et al2 in 1998, they showed an ascending thoracic pseudoaneurysm in a patient who presented with purulent pericarditis, which is similar to the present case report. There also have been documented cases of staphylococcus aortitis leading to pseudoaneurysm formation. This patient likely developed a pseudoaneurysm secondary to his recurrent methicillin-sensitive S aureus pericarditis and/or repeated pericardial surgeries. With the patient having significant symptoms over an extended time period with unresolving pericarditis despite appropriate treatment and recurring pericardial effusions, it is most likely that the infectious pericarditis was the precipitating event or an atheromatous ulcer became infected causing the pseudoaneurysm. A chest CT scan, magnetic resonance imaging, aortography, and transesophageal echocardiography are very reliable in detecting aortic pseudoaneurysms, and TEE has been shown to be highly sensitive and specific for diagnosing pseudoaneurysm formation. Transthoracic echocardiography is a less reliable method for diagnosing thoracic pseudoaneurysm because there
1100
INGOGLIA ET AL
frequently can be interference from the lung, ribs, and subcutaneous tissues depending on the patient’s body habitus. The TEE affords much better resolution because transduction is not obscured by dense surrounding tissues and its relative proximity to the ascending aorta.7 In a patient who has had cardiac surgery, regardless of how remote, who presents with chest pain and other related symptoms that cannot be explained by electrocardiogram and laboratory findings should be further investigated, especially if any
of the afore mentioned symptoms are present. Nonresolving pericarditis after an extended treatment course may warrant imaging studies other than a TTE to gain clear visualization of the heart and surrounding structures that a TTE can miss. Although the incidence of thoracic pseudoaneurysm formation in patients without prior cardiac surgery is very low, pseudoaneurysm should be a consideration after other more common diagnoses are excluded.
REFERENCES 1. Dumont E, Carrier M, Cartier R, et al: Repair of aortic false aneurysm using deep hypothermic and circulatory arrest. Ann Thorac Surg 78:117-120, 2004 2. Aranda J, Tauth J, Henning RJ, et al: Pseudoaneurysm of the thoracic aorta presenting as purulent pericarditis and pericardial effusion. Cathet Cardiovasc Diagn 43:63-67, 1998 3. Sequeira de Almeida RM, Limas JD, Kahrbek T, et al: Surgical repair of a pseudoaneurysm of the ascending aorta after aortic valve replacement. Arq Bras Cardiol 76:326-328, 2001
4. Sullivan KL, Steiner RM, Smullens SL, et al: Pseudoaneurysm of the ascending aorta following cardiac surgery. Chest 93:138-143, 1988 5. Konia M, Uppington J, Moore P, et al: Ascending aortic pseudoaneurysm: A late complication of coronary artery bypass. Anesth Analg 106:767-768, 2008 6. Atik FA, Navia JL, Svensson LG, et al: Surgical treatment of pseudoaneurysm of the thoracic aorta. J Thorac Cardiovasc Surg 132:379385, 2006 7. Lobato EB, McKenzie ED, Beaver TM: Intraoperative diagnosis of aortic pseudoaneurysm with transesophageal echocardiography. J Clinical Monit Comput 15:53-55, 1999